George A Kaysen1, Burl R Don. 1. Department of Veterans Affairs Northern California Health Care System, Mather, CA, USA. gakaysen@ucdavis.edu
Abstract
INTRODUCTION: Hypoalbuminemia is a powerful risk factor for cardiovascular mortality in hemodialysis patients (HD). Inflammation causes a decrease in albumin synthesis and an increase in albumin fractional catabolic rate, providing two mechanisms for hypoalbuminemia. The inflammatory response alters the endothelium and plasma protein composition in ways that favor vascular injury. Plasma volume is expanded in HD patients, providing another mechanism for hypoalbuminemia. Fibrinogen levels are an independent risk factor for cardiovascular disease (CVD) in HD patients, and fibrinogen levels are increased in HD patients. Plasma volume expansion is also an independent risk factor for CVD. METHODS: Albumin synthesis was measured in 74 HD patients as the disappearance of [125I] human albumin over six weeks. Fibrinogen was measured in plasma. Plasma fibrinogen mass was the product of fibrinogen concentration and plasma volume. RESULTS: Albumin synthesis correlated positively with plasma volume (P < 0.001). Fibrinogen concentration and plasma fibrinogen mass both correlated positively with albumin synthesis (P < 0.001). CONCLUSION: Albumin levels are reduced as part of the acute-phase response in HD. Plasma volume expansion also tends to decrease albumin concentration, but elicits an increase in its rate of synthesis, which, in turn, is associated with increased fibrinogen levels. Thus, both inflammation and plasma volume expansion factors that reduce albumin concentration and are independent cardiovascular risk factors, independently increase fibrinogen levels.
INTRODUCTION:Hypoalbuminemia is a powerful risk factor for cardiovascular mortality in hemodialysis patients (HD). Inflammation causes a decrease in albumin synthesis and an increase in albumin fractional catabolic rate, providing two mechanisms for hypoalbuminemia. The inflammatory response alters the endothelium and plasma protein composition in ways that favor vascular injury. Plasma volume is expanded in HDpatients, providing another mechanism for hypoalbuminemia. Fibrinogen levels are an independent risk factor for cardiovascular disease (CVD) in HDpatients, and fibrinogen levels are increased in HDpatients. Plasma volume expansion is also an independent risk factor for CVD. METHODS: Albumin synthesis was measured in 74 HDpatients as the disappearance of [125I] human albumin over six weeks. Fibrinogen was measured in plasma. Plasma fibrinogen mass was the product of fibrinogen concentration and plasma volume. RESULTS: Albumin synthesis correlated positively with plasma volume (P < 0.001). Fibrinogen concentration and plasma fibrinogen mass both correlated positively with albumin synthesis (P < 0.001). CONCLUSION: Albumin levels are reduced as part of the acute-phase response in HD. Plasma volume expansion also tends to decrease albumin concentration, but elicits an increase in its rate of synthesis, which, in turn, is associated with increased fibrinogen levels. Thus, both inflammation and plasma volume expansion factors that reduce albumin concentration and are independent cardiovascular risk factors, independently increase fibrinogen levels.
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